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None of the mutations observed in the coronavirus to date appear to be helping it spread from person to person, research suggests.
Scientists from University College London (UCL) analysed the virus’ genetics in more than 46,000 people with a confirmed infection from 99 countries.
More than 12,000 mutations were recorded in total. The scientists honed in on 185 of the genetic changes that occurred at least three times in separate patients over the pandemic.
The scientists then modelled the virus’ evolutionary tree, analysing whether after a mutation comes about, the viral descendants of that infection outperform closely-related strains without the genetic change.
Results revealed there is no evidence any of the common mutations are increasing the virus’ transmissibility, with the majority having a neutral effect.
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“The number of [coronavirus] genomes [all the genetic material of an organism] being generated for scientific research is staggering,” said study author Dr Lucy van Dorp.
“We realised early on in the pandemic we needed new approaches to analyse enormous amounts of data in close to real time to flag new mutations in the virus that could affect its transmission or symptom severity.
“Fortunately, we found none of these mutations are making COVID-19 [the disease caused by the coronavirus] spread more rapidly, but we need to remain vigilant and continue monitoring new mutations, particularly as vaccines get rolled out.”
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Early in the coronavirus outbreak, concerns were raised the infection could evolve to become more contagious or dangerous.
The coronavirus is an RNA virus, which mutate almost constantly. That being said, the coronavirus reportedly changes at a relatively low rate compared to other RNA viruses, like HIV. In simple terms, RNA is a precursor to the more well-known DNA.
An RNA virus can develop mutations by mistake if it copies an error while replicating. It can also interact with another virus infecting the same cell, picking up its mutations. Genetic changes can also come about as a result of the patient’s immune response against the virus.
Most mutations are neutral, while others can be advantageous or detrimental to the virus.
Neutral and advantageous mutations can become more common as they get passed to descendant viruses. Detrimental mutations tend not to “stick”; think survival of the fittest.
To better understand the impact of coronavirus mutations, the UCL scientists analysed tens of thousands of patients’ viral genomes up to the end of July.
Of the more 12,000 mutations that were identified, 398 had “strong evidence” of occurring repeatedly and independently in individual coronaviruses.
The scientists then honed in on the 185 mutations that occurred independently at least three times.
After mapping these genetic changes on the evolutionary tree, the scientists found no evidence the mutations are helping the virus spread.
Most of the genetic changes were neutral, including the widely-reported D614G mutation to the virus’ spike protein.
The coronavirus uses its spike protein to invade cells, with scientists from the Los Alamos National Laboratory in New Mexico previously calling the D614G mutation “of urgent concern”.
The UCL results – published in the journal Nature Communications – further revealed the coronavirus’ common mutations appear to have been induced by the human immune system, rather than the virus adapting to its host.
This is in contrast to a separate analysis by the same UCL team, who investigated how the coronavirus jumped from humans into farmed minks.
Outbreaks have emerged on several mink farms worldwide. The infection was thought to have passed from farmers into the animals and then occasionally back into humans, raising the risk the virus will mutate.
“When we analysed virus genomes sourced from mink, we were amazed to see the same mutation appearing over and again in different mink farms, despite those same mutations having rarely been observed in humans before,” said Dr van Dorp.
These mutations may have occurred in humans before the coronavirus started hitting the headlines.
“We previously estimated [the coronavirus] jumped into humans in October or November 2019, but the first genomes we have date to the very end of December,” said lead author Professor Francois Balloux.
“By that time, viral mutations crucial for the transmissibility in humans may have emerged and become fixed, precluding us from studying them.”
Viruses are expected to mutate, however, this does not necessarily mean they become more transmissible or dangerous.
“The virus seems well adapted to transmission among humans, and it may have already reached its fitness optimum in the human host by the time it was identified as a novel virus,” said Professor Balloux.
As well as concerns about how genetic changes may affect transmission, some have worried the virus may evolve to evade immunisation, with many vaccine candidates targeting the infection’s spike protein.
The scientists stressed, however, the computer model they have developed should identify any vaccine-related mutations in plenty of time.
“The virus may well acquire vaccine-escape mutations in the future, but we’re confident we’ll be able to flag them up promptly, which would allow updating the vaccines in time if required,” said Professor Balloux.
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This is not the first time coronavirus mutations have been discussed.
In March, scientists from Peking University in Beijing claimed two major types of the coronavirus had evolved, with the more “aggressive” strain being the most widespread.
A team from the University of Glasgow then “examined in detail” the data presented by the Beijing scientists, concluding it “cannot be substantiated”.
Writing on Twitter, Professor Andrew Rambaut from the University of Edinburgh said genetic variations are “entirely expected”.
He added it is a “flawed inference” to suggest the mutations could make the virus behave differently.
Some have argued the virus does not need to evolve to become more transmissible, with tens of millions already confirmed to have been infected worldwide.
“At our cost the virus is doing well enough colonising the human population,” Professor Ian Jones from the University of Reading previously said.
Dr William Hanage from Harvard added: “Essentially the virus has been mutating. That don’t mean that much.
“Mutations are what happens when genomes replicate.
“Comes with the territory, like showers with the springtime.”
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